Microbiological and Immunological Aspects of Experimental Periodontal Disease in Rats: A Review Article

Klausen, Bjarne

doi:10.1902/jop.1991.62.1.59

Cited by 165 publications

(153 citation statements)

References 70 publications

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“…Among other important variations that could affect conclusions drawn from animal models, nonhuman animals differ from humans in anatomy, immune response, and lifestyle. For the study of periodontal disease, mice (25,33,34,(37)(38)(39), rats (36,40,41), and nonhuman primates (42)(43)(44) have been most frequently used. While primates closely resemble humans with regard to anatomy and physiology, their cost, size, and maintenance requirements prohibit studies with large samples.…”

Section: Discussionmentioning

confidence: 99%

Tight-adherence genes of Actinobacillus actinomycetemcomitans are required for virulence in a rat model

Schreiner

Sinatra

Kaplan

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

150

165

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Actinobacillus actinomycetemcomitans is a Gram-negative coccobacillus that has been associated with localized aggressive periodontitis and infections of the heart, brain, and urinary tract. Wild-type clinical isolates have the remarkable ability to adhere tenaciously and nonspecifically to solid surfaces such as glass, plastic, and hydroxyapatite. Adherence by A. actinomycetemcomitans is mediated by the tight-adherence (tad) gene locus, which consists of 14 genes (flp-1-flp-2-tadV-rcpCAB-tadZABCDEFG). All but 2 of the genes have been shown to be required for the secretion and assembly of long, bundled Flp1 fibrils. To test whether the tad locus is required for colonization and disease, we developed a rat model for periodontal disease. To mimic the natural route of infection, Sprague-Dawley rats were inoculated orally by adding bacteria directly to their food for 8 days. After inoculation with wild-type or mutant strains defective in adherence (flp-1 and tadA), the rats were assessed for colonization of the oral cavity and pathogenesis. Wild-type A. actinomycetemcomitans was able to colonize and persist for at least 12 weeks in the oral cavity, elicit a humoral immune response, and cause significant bone loss in rats. In contrast, rats fed flp-1 or tadA mutant strains showed no bone loss and their immune responses were indistinguishable from those of the uninoculated controls. These results demonstrate the critical importance of the tad locus in the colonization and pathogenesis of A. actinomycetemcomitans. nonspecific adherence ͉ tad genes ͉ pathogenesis ͉ localized juvenile periodontitis

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Section: Discussionmentioning

confidence: 99%

Tight-adherence genes of Actinobacillus actinomycetemcomitans are required for virulence in a rat model

Schreiner

Sinatra

Kaplan

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

150

165

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“…Rats are suitable for study of the effects of systemic diseases and pharmacological therapies on tissue destruction and regeneration (Graves et al, 2008), and for evaluation of physiological alterations related to aging (Benatti et al, 2006). In addition, tissue destruction and regeneration in an immunodeficient background can be investigated in this model (Klausen, 1991). Surgery and the evaluation of study endpoints are challenging, however, because of the animals' small size.…”

Section: Rat As a Candidate Small-defect Modelmentioning

confidence: 99%

Pre-clinical Models for Oral and Periodontal Reconstructive Therapies

et al. 2009

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The development of new medical formulations (NMF) for reconstructive therapies has considerably improved the available treatment options for individuals requiring periodontal repair or oral implant rehabilitation. Progress in tissue engineering and regenerative medicine modalities strongly depends on validated pre-clinical research. Preclinical testing has contributed to the recent approval of NMF such as GEM 21S ® and INFUSE ® bone grafts for periodontal and oral regenerative therapies. However, the selection of a suitable preclinical model for evaluation of the safety and efficacy of a NMF remains a challenge. This review is designed to serve as a primer to choose the appropriate pre-clinical models for the evaluation of NMF in situations requiring periodontal or oral reconstruction. Here, we summarize commonly used pre-clinical models and provide examples of screening and functional studies of NMF that can be translated into clinical use.

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“…In order to characterize P. gingivalishost interactions a number of animal infection models have been developed, the most common of which are rodent models (6,20,25,28,40,44). Rodent models have been used to identify P. gingivalis components that are involved in pathogenesis (26,32,43,46,48,52,56,57,67,73) and to characterize the host response to P. gingivalis infection (3,6,7,13,22,31,34,35,41,74).…”

mentioning

confidence: 99%

Porphyromonas gingivalis-Host Interactions in aDrosophila melanogasterModel

et al. 2011

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Porphyromonas gingivalis is a Gram-negative obligate anaerobe that has been implicated in the etiology of adult periodontitis. We recently introduced a Drosophila melanogaster killing model for examination of P. gingivalis-host interactions. In the current study, the Drosophila killing model was used to characterize the host response to P. gingivalis infection by identifying host components that play a role during infection. Drosophila immune response gene mutants were screened for altered susceptibility to killing by P. gingivalis. The Imd signaling pathway was shown to be important for the survival of Drosophila infected by nonencapsulated P. gingivalis strains but was dispensable for the survival of Drosophila infected by encapsulated P. gingivalis strains. The P. gingivalis capsule was shown to mediate resistance to killing by Drosophila antimicrobial peptides (Imd pathway-regulated cecropinA and drosocin) and human beta-defensin 3. Drosophila thiol-ester protein II (Tep II) and Tep IV and the tumor necrosis factor (TNF) homolog Eiger were also involved in the immune response against P. gingivalis infection, while the scavenger receptors Eater and Croquemort played no roles in the response to P. gingivalis infection. This study demonstrates that the Drosophila killing model is a useful high-throughput model for characterizing the host response to P. gingivalis infection and uncovering novel interactions between the bacterium and the host.Porphyromonas gingivalis is a Gram-negative, obligate anaerobe that has been strongly implicated as a pathogen in adult (chronic) periodontitis (23, 29), a polymicrobial inflammatory disease that affects the gingiva and other toothsupporting structures. In order to characterize P. gingivalishost interactions a number of animal infection models have been developed, the most common of which are rodent models (6,20,25,28,40,44). Rodent models have been used to identify P. gingivalis components that are involved in pathogenesis (26,32,43,46,48,52,56,57,67,73) and to characterize the host response to P. gingivalis infection (3,6,7,13,22,31,34,35,41,74).The use of the fruit fly Drosophila melanogaster has been well established for examining host-pathogen interactions (5,16,19,21,53,55,65,66). Numerous studies have demonstrated the high degree of conservation between the Drosophila immune system and the mammalian innate immune system (reviewed in reference 49). Like the mammalian innate immune system, the Drosophila immune system detects the presence of invading microbes by using pattern recognition receptors (PRRs), which recognize pathogen-associated molecular patterns (PAMPs) and trigger an immune response that is specific for the class of invading microbe. Other mammalian immune response features that are conserved in Drosophila include signaling pathways (e.g., Toll/interleukin-1 receptor [IL1R], tumor necrosis factor receptor [TNFR]), antimicrobial peptides (AMPs), macrophage-like blood cells, complement C3/ ␣ 2 -macroglobulin (C3/␣ 2 M) superfamily proteins, cytokines, react...

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Microbiological and Immunological Aspects of Experimental Periodontal Disease in Rats: A Review Article

Cited by 165 publications

References 70 publications

Tight-adherence genes of Actinobacillus actinomycetemcomitans are required for virulence in a rat model

Tight-adherence genes of Actinobacillus actinomycetemcomitans are required for virulence in a rat model

Pre-clinical Models for Oral and Periodontal Reconstructive Therapies

Porphyromonas gingivalis-Host Interactions in aDrosophila melanogasterModel

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